UIC-2019-182 Treatment for ARDS using EB3 Inhibitors

ARDS is characterized by the rapid onset of pulmonary inflammation leading to persistent, widespread pulmonary edema and fibrosis causing severe shortness of breath and hypoxia that can progress towards multiorgan failure and death. Restoration of the endothelial barrier may lead to resolution of ARDS, however, no current therapeutics adequately address endothelial hyper-permeability associated with ARDS. Microtubule-associated protein RP/EB family member 3 – also known as End Binding protein 3 (EB3) has been implicated in pulmonary edema by regulating pathological calcium signals in endothelial cells. UIC Solution UIC inventors discovered a lead therapeutic peptide candidate, UIC-109, that inhibits EB3 function, combats ARDS through suppression of pathological pulmonary vascular leakage, and reduces systemic inflammation and organ failure. UIC-109 demonstrates superior activity, cell-penetration, and stability both in vitro human blood plasma and in vivo murine models.Treatment of mice with UIC-109 restores tissue-fluid homeostasis in severely injured lungs and markedly improves survival of mice in a sepsis model of ARDS. Importantly, UIC-109 also prevents both the development of pulmonary fibrosis associated with ARDS and high-volume mechanical ventilation-induced lung injury. Veronica Haywood vhaywo2@uic.otm.edu 312-996-4865

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